98%
921
2 minutes
20
Background: The odontogenic keratocyst (OKC) corresponds to the third most common odontogenic cyst of the maxillary bones, originating from the dental lamina or its remnants. Apoptosis dysregulation, due to an imbalance between anti-apoptotic and proapoptotic proteins, has been proposed as a promoter for the development and progression of OKC. This study aimed to conduct a systematic review to synthesize the current knowledge on effector proteins of the intrinsic and extrinsic pathways, and executor proteins of apoptosis in OKC and compare their expression to other odontogenic cysts and tumors.
Material And Methods: Primary studies were searched in PubMed, Scopus, and Web of Science databases, following the recommendations of PRISMA. Inclusion criteria were articles in English reporting the expression of at least two apoptosis-related proteins in OKC, studies using human tissues, descriptive retrospective case series, or in vitro assays.
Results: Seven articles met the inclusion criteria and were considered for data extraction and analysis. Of the selected articles, six studied proteins related to the regulation of the intrinsic pathway of apoptosis, all reporting the immunohistochemical expression of Bcl-2 and BAX. Only one study reported the immunohistochemical expression of proteins related to the regulation of the extrinsic pathway, specifically Fas and FasL. Regarding apoptosis execution proteins, only one article characterized the immunohistochemical expression of caspases, specifically caspase-3.
Conclusions: OKC expresses proteins related to apoptosis regulation similar to other aggressive odontogenic lesions, such as ameloblastoma. This suggests that apoptosis dysregulation may be essential in its development and progression.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC12395592 | PMC |
http://dx.doi.org/10.4317/medoral.26973 | DOI Listing |
Mutat Res Rev Mutat Res
September 2025
Institute of Environmental Medicine, Zhejiang University School of Medicine, Hangzhou 310058, China. Electronic address:
To maintain genomic stability, cells have evolved complex mechanisms collectively known as the DNA damage response (DDR), which includes DNA repair, cell cycle checkpoints, apoptosis, and gene expression regulation. Recent studies have revealed that long non-coding RNAs (lncRNAs) are pivotal regulators of the DDR. Beyond their established roles in recruiting repair proteins and modulating gene expression, emerging evidence highlights two particularly intriguing functions.
View Article and Find Full Text PDFPhysiology (Bethesda)
September 2025
Departments of Ophthalmology and Medicine, Stanford Cardiovascular Institute, Stanford University, Palo Alto, CA 94304.
Canonical activation of G-protein coupled receptors (GPCRs) by hormone binding occurs at the plasma membrane, resulting in the diffusion of second messengers to intracellular effector sites throughout the cell. In contrast, recent evidence suggests that functional GPCRs can induce signaling from distinct intracellular domains, contributing to specificity in signaling. Functional adrenergic receptors have been identified at intracellular sites in the cardiac myocyte such as endosomes, the sarcoplasmic reticulum, the Golgi and the inner nuclear membrane.
View Article and Find Full Text PDFSci Transl Med
September 2025
Department of Medicine, Columbia University Irving Medical Center, New York, NY 10032, USA.
Hepatocyte apoptosis is a key feature of metabolic dysfunction-associated steatohepatitis (MASH), but the fate of apoptotic hepatocytes in MASH is poorly understood. Here, we explore the hypotheses that clearance of dead hepatocytes by liver macrophages (efferocytosis) is impaired in MASH because of low expression of the efferocytosis receptor T cell immunoglobulin and mucin domain containing 4 (TIM4; gene ) by MASH liver macrophages, which then drives liver fibrosis in MASH. We show that apoptotic hepatocytes accumulate in human and experimental MASH, using mice fed the fructose-palmitate-cholesterol (FPC) diet or the high-fat, choline-deficient amino acid-defined (HF-CDAA) diet.
View Article and Find Full Text PDFExp Physiol
September 2025
Department of Hepatobiliary Surgery, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, Huaian, Jiangsu, China.
Hepatic ischaemia-reperfusion (IR) injury is a serious clinical issue, especially in patients with type 2 diabetes mellitus (T2DM). As mitochondria play a critical role in the regulation of IR-induced liver damage, mitochondria-targeted treatment is of the utmost significance for improving outcomes. The present study explored the mitoprotective role of combined ginsenoside-MC1 (GMC1) and irisin administration in diabetic rats with hepatic IR injury.
View Article and Find Full Text PDFPLoS One
September 2025
Department of Cardiac Surgery, Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany.
Background: Cardiac ischemia reperfusion (I/R) injury is a serious consequence of reperfusion therapy for myocardial infarction (MI). Peptidylarginine deiminase 4 (PAD4) is a calcium-dependent enzyme that catalyzes the citrullination of proteins. In previous studies, PAD4 inhibition protected distinct organs from I/R injury by preventing the formation of neutrophil extracellular traps (NETs) and attenuating inflammatory responses.
View Article and Find Full Text PDF